Alzheimer's disease (AD) affects more than 35 million people worldwide and costs more than 170 billion dollars to treat and manage in the U.S. alone. AD is a slowly progressing disease characterized by the overproduction of amyloid beta (Aβ) peptide in neuronal tissue. While the exact mode of action of Aβ peptide is unclear, overproduction ultimately leads to neuron death and the clinical symptoms of AD. The complexity of AD and the significant public health issue it poses demands the exploration of a variety of novel strategies that hold promise for effective diagnosis and treatment.
Current treatments for AD treat the symptoms but do not treat the underlying disease, and have only modest effects on patient outcome. Current strategies to treat the disease have focused on relieving the amyloid burden through the inhibition of the gamma secretase complex or anti-amyloid antibodies. To date these strategies have failed to achieve significant improvements in patient outcome despite a number of large phase III clinical trials. Emerging therapeutic strategies include attempts to limit tau tangles as well as metabolic interventions. None of these strategies are focused on a direct molecular target of Aβ but rather downstream cellular effects of excess Aβ.
There remains a need to identify steps in the causation of the symptoms of Alzheimer's disease, to develop diagnostics to identify afflicted patients, and to develop therapeutic strategies to address them.